The aetiology of
complex regional pain syndrome (CRPS), a highly painful, usually post-traumatic condition affecting the limbs, is unknown, but recent results have suggested an autoimmune contribution. To confirm a role for pathogenic
autoantibodies, we established a passive-transfer
trauma model. Prior to undergoing incision of hind limb plantar skin and muscle, mice were injected either with serum
IgG obtained from chronic CRPS patients or matched healthy volunteers, or with saline. Unilateral hind limb plantar skin and muscle incision was performed to induce typical, mild tissue injury.
Mechanical hyperalgesia, paw swelling, heat and cold sensitivity, weight-bearing ability, locomotor activity, motor coordination, paw temperature, and
body weight were investigated for 8days. After sacrifice, proinflammatory sensory
neuropeptides and
cytokines were measured in paw tissues. CRPS patient
IgG treatment significantly increased hind limb
mechanical hyperalgesia and oedema in the incised paw compared with
IgG from healthy subjects or saline. Plantar incision induced a remarkable elevation of
substance P immunoreactivity on day 8, which was significantly increased by CRPS-
IgG. In this
IgG-transfer-
trauma model for CRPS, serum
IgG from chronic CRPS patients induced clinical and laboratory features resembling the human disease. These results support the hypothesis that
autoantibodies may contribute to the pathophysiology of CRPS, and that
autoantibody-removing
therapies may be effective treatments for long-standing CRPS.